Anopheles stephensi, a mosquito species non-native to Africa, is spreading across the continent, complicating malaria-control efforts. How big a threat are these mosquitoes? Harvard Chan School's…

Current licensed malaria vaccines are modestly protective against severe Plasmodium falciparum malaria but do not contain components which control blood stage infection. We evaluated the impact of antibodies to three blood stage candidate antigens (PfGARP, PfSEA-1, and PfGBP130) on P. falciparum infection and disease in a longitudinal cohort of children living in a holoendemic region of Western Kenya.MethodsWe enrolled and followed 266 children aged 2 to 7 years living in Western Kenya. Over the course of a 3-year follow-up period, we actively assessed their health status weekly, collected blood samples monthly to assess P. falciparum infection incidence and intensity, and measure IgG antibody levels to blood stage vaccine candidate antigens.ResultsChildren with high levels of IgG antibodies to PfGBP130 or PfGARP, but not PfSEA-1, experienced 3.4- and 1.9- fold lower parasite densities respectively compared to those with low antibody levels (both P < 0.002). In addition, children with high levels of both anti-PfGBP130 and anti-PfGARP had significantly lower risk of clinical malaria compared to children with low antibody levels (HR: 0.58, 95% CI: 0.85-0.40). Over the 3-year follow-up period, individuals with elevated anti-PfGBP130 and anti-PfGARP antibody levels experienced an average of 4.51 cases of clinical malaria while those with lower levels experienced an average of 7.11 cases of clinical malaria (P = 0.005).ConclusionsHigher antibody levels to PfGBP130 and PfGARP predict significantly lower parasite densities and lower risks of clinical malaria among 2- to 7-year-old children residing in a holoendemic area of Kenya.

A study led by Brown University researchers has identified a genetic mutation called PIN that is contributing to the rapid spread of drug-resistant malaria in sub-Saharan Africa. The mutation, which affects the px1 gene, was found in 84% of malaria parasite samples from northern Uganda and 55% from eastern Uganda by 2024. This mutation reduces sensitivity to lumefantrine, a key component of the artemether-lumefantrine drug combination. The PIN mutation emerged around 2008 and spread rapidly, outpacing genetic recombination processes. Parasites with this mutation showed stronger resistance to certain antimalarials compared to those without it. While previous research linked Kelch13 (K13) mutations to artemisinin resistance, the PIN mutation provides the first validated marker for lumefantrine resistance. The study highlights urgent needs for improved surveillance systems and new treatments as drug resistance threatens malaria control efforts in Africa and beyond.

Wissenschaftlerinnen und Wissenschaftler der Medizinischen Fakultät der Universität Heidelberg, des Zentrums für Infektiologie des Universitätsklinikums Heidelberg und des Deutschen Z